Progress 10/01/12 to 09/30/13
Outputs
Progress Report Objectives (from AD-416): Maintaining gut microbiota in developing chickens is critical for animal health. Gut microbiota plays an important role in innate immunity and disruption in gut normal flora during infectious diseases needs to be better studied in order to understand host-pathogen interaction in necrotic enteritis. Cooperators will access gut microbiota in the intestinal samples which will be collected from experimental disease models developed at ARS. Approach (from AD-416): Reliable disease models for necrotic enteritis will be developed. Intestinal samples from various parts of the chicken intestine will be collected at different time points following the disease challenge by using an established necrotic enteritis disease model. DNA samples will be prepared and sent to the Cooperator for gut microbiota analysis using pyrosequencing. Necrotic enteritis which is caused by an intestinal bacteria, Clostridium perfringens inflicts substantial economic losses in commercially-bred broilers worldwide. Recent studies showed that Clostridium perfringens infection of chickens disrupts the normal gut microflora (dysbiosis). A change of the bacterial populations in the gut may contribute to the pathogenesis of Necrotic enteritis. Therefore, we investigated alterations in intestinal bacterial communities in three commercial breeds of broiler chickens (Cobb, Ross, and Hubbard) that differ in susceptibility to experimental Necrotic enteritis. The three chicken breeds showed different gut bacteria profiles. In general, the diversity of bacterial genus in all three chicken breeds was reduced following a single or double infections with Clostridium perfringens compared with uninfected controls. Furthermore, differences were observed in the microbial community profiles at the genus and species levels among the different breeds. This was also true when comparing uninfected versus infected and a single infection with either the Clostridium perfringens bacterium or Eimeria maxima parasite versus co-infections with Clostridium perfringens/Eimeria maxima. These new findings increased our understanding of the nature of intestinal dysregulation of its bacterial population occurring during experimental Necrotic enteriris in birds. It also demonstrated the inherent genetic differences in the dynamic changes of gut microbial communities in Necrotic enteritis-afflicted commercial poultry flocks.
Impacts
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Progress 10/01/11 to 09/30/12
Outputs
Progress Report Objectives (from AD-416): Maintaining gut microbiota in developing chickens is critical for animal health. Gut microbiota plays an important role in innate immunity and disruption in gut normal flora during infectious diseases needs to be better studied in order to understand host-pathogen interaction in necrotic enteritis. Cooperators will access gut microbiota in the intestinal samples which will be collected from experimental disease models developed at ARS. Approach (from AD-416): Reliable disease models for necrotic enteritis will be developed. Intestinal samples from various parts of the chicken intestine will be collected at different time points following the disease challenge by using an established necrotic enteritis disease model. DNA samples will be prepared and sent to the Cooperator for gut microbiota analysis using pyrosequencing. Avian coccidiosis and necrotic enteritis are among the most economically significant diseases affecting the poultry industry worldwide. Two commercial broiler chickens (C and R) were induced to develop necrotic enteritis using an Eimeria maxima and Clostridium perfringens co- infection model that our laboratory previously developed. Two days post- infection, total genomic DNA was extracted from the ileal contents and sequenced to obtain pooled samples of a specific region (V1 to V3) of a specific gene (16S) for bacterial ribosomal RNA. More than 60,000 partial 16S ribosomal DNA sequences that were obtained from 50 ileal samples are being analyzed using a bioinformatics program to assess the microbial populations.
Impacts
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